169 Ch 20_lecture_presentation

© 2012 Pearson Education, Inc.
PowerPoint®
Lecture Presentations prepared by
Jason LaPres
Lone Star College—North Harris
20
The Heart

An Introduction to the Cardiovascular System
• Learning Outcomes
• 20-1 Describe the anatomy of the heart, including
vascular supply and pericardium structure, and
trace the flow of blood through the heart,
identifying the major blood vessels, chambers,
and heart valves.
• 20-2 Explain the events of an action potential in
cardiac muscle, indicate the importance of
calcium ions to the contractile process, describe
the conducting system of the heart, and identify
the electrical events associated with a normal
electrocardiogram.

• Learning Outcomes
• 20-3 Explain the events of the cardiac cycle,
including atrial and ventricular systole and
diastole, and relate the heart sounds to specific
events in the cycle.
• 20-4 Define cardiac output, describe the factors that
influence heart rate and stroke volume, and
explain how adjustments in stroke volume and
cardiac output are coordinated at different levels
of physical activity.

• The Pulmonary Circuit
• Carries blood to and from gas exchange surfaces of
lungs
• The Systemic Circuit
• Carries blood to and from the body
• Blood alternates between pulmonary circuit and
systemic circuit

• Three Types of Blood Vessels
1. Arteries
• Carry blood away from heart
2. Veins
• Carry blood to heart
3. Capillaries
• Networks between arteries and veins

• Capillaries
• Also called exchange vessels
• Exchange materials between blood and tissues
• Materials include dissolved gases, nutrients, waste
products

Figure 20-1 An Overview of the Cardiovascular System
PULMONARY CIRCUIT SYSTEMIC CIRCUIT
Pulmonary arteries
Pulmonary veins Systemic veins
Systemic arteries
Capillaries
in lungs
Right
atrium
Right
ventricle
Capillaries
in trunk
and lower
limbs
Capillaries
in head,
neck, upper
limbs
Left
atrium
Left
ventricle

• Four Chambers of the Heart
1. Right atrium
• Collects blood from systemic circuit
2. Right ventricle
• Pumps blood to pulmonary circuit
3. Left atrium
• Collects blood from pulmonary circuit
4. Left ventricle
• Pumps blood to systemic circuit

20-1 Anatomy of the Heart
• The Heart
• Great veins and arteries at the base
• Pointed tip is apex
• Surrounded by pericardial sac
• Sits between two pleural cavities in the mediastinum

Figure 20-2a The Location of the Heart in the Thoracic Cavity
Trachea
First rib (cut)
Base of heart
Right lung
Diaphragm
Thyroid gland
Left lung
Apex of heart
Parietal pericardium
(cut)
An anterior view of the chest, showing the position of the heart and
major blood vessels relative to the ribs, lungs, and diaphragm.

• The Pericardium
• Double lining of the pericardial cavity
• Visceral pericardium
• Inner layer of pericardium
• Parietal pericardium
• Outer layer
• Forms inner layer of pericardial sac

• The Pericardium
• Pericardial cavity
• Is between parietal and visceral layers
• Contains pericardial fluid
• Pericardial sac
• Fibrous tissue
• Surrounds and stabilizes heart

Figure 20-2b The Location of the Heart in the Thoracic Cavity
Right ventricle
Aortic
arch
Posterior mediastinum
Aorta (arch segment removed)
Left pulmonary artery
Left pulmonary vein
Pulmonary trunk
Left ventricle
Epicardium
Pericardial sac
Anterior mediastinum
Pericardial cavity
Right atrium
Left atrium
Right pulmonary artery
Right pulmonary vein
Superior vena cava
Esophagus
Right pleural cavity
Bronchus of lung
Right
lung Left
lung
Left pleural cavity
A superior view of the organs in the mediastinum; portions of the lungs have
been removed to reveal blood vessels and airways. The heart is situated in
the anterior part of the mediastinum, immediately posterior to the sternum.

Figure 20-2c The Location of the Heart in the Thoracic Cavity
Wrist (corresponds
to base of heart)
Inner wall (corresponds
to epicardium)
Air space (corresponds
to pericardial cavity)
Outer wall (corresponds
to parietal pericardium)
Balloon
Cut edge of
parietal pericardium
Fibrous tissue of
pericardial sac
Areolar tissue
Mesothelium
Cut edge of epicardium
Apex of heart
Base of heart
Fibrous
attachment
to diaphragm
The relationship between the heart and the pericardial cavity; compare with the fist-and-balloon example.

• Superficial Anatomy of the Heart
• Atria
• Thin-walled
• Expandable outer auricle (atrial appendage)

• Superficial Anatomy of the Heart
• Sulci
• Coronary sulcus divides atria and ventricles
• Anterior interventricular sulcus and posterior
interventricular sulcus
• Separate left and right ventricles
• Contain blood vessels of cardiac muscle

Figure 20-3a The Superficial Anatomy of the Heart
Left common
carotid artery
Brachiocephalic
trunk
Ascending
aorta
Superior
vena cava
Auricle
of right
atrium
Fat and
vessels in
coronary
sulcus
Left subclavian artery
Arch of aorta
Ligamentum
arteriosum
Descending
aorta
Left pulmonary
artery
Pulmonary
trunk
Auricle of
left atrium
Fat and vessels
in anterior
interventricular
sulcus
LEFT
VENTRICLE
RIGHT
VENTRICLE
RIGHT
ATRIUM
Major anatomical features on the anterior surface.

Figure 20-3a The Superficial Anatomy of the Heart
Ascending
aorta
Parietal
pericardium
Superior
vena cava
Auricle of
right atrium
RIGHT ATRIUM
Right coronary
artery
Coronary sulcus
RIGHT VENTRICLE
Marginal branch
of right coronary artery
Auricle of
left atrium
Pulmonary
trunk
Fibrous
pericardium
fused to diaphragm
Anterior
interventricular
sulcus
LEFT
VENTRICLE
Major anatomical features on the anterior surface.

Figure 20-3b The Superficial Anatomy of the Heart
Arch of aorta
Right pulmonary
artery
Superior
vena cava
Right
pulmonary
veins (superior
and inferior)
Inferior
vena cava
Fat and vessels in posterior
RIGHT
VENTRICLE
LEFT
VENTRICLE
RIGHT
ATRIUM
LEFT
ATRIUM
Left pulmonary artery
Left pulmonary veins
Fat and vessels in
coronary sulcus
Coronary
sinus
Major landmarks on the posterior surface. Coronary
arteries (which supply the heart itself) are shown in
red; coronary veins are shown in blue.

Figure 20-3c The Superficial Anatomy of the Heart
Base of heart
Apex of
heart
Ribs
Heart position relative to the rib cage.
1
2
3
4
5
6
7
8
9
10
1
2
3
4
5
6
7
8
9
10

• The Heart Wall
1. Epicardium
2. Myocardium
3. Endocardium

• Epicardium (Outer Layer)
• Visceral pericardium
• Covers the heart

• Myocardium (Middle Layer)
• Muscular wall of the heart
• Concentric layers of cardiac muscle tissue
• Atrial myocardium wraps around great vessels
• Two divisions of ventricular myocardium
• Endocardium (Inner Layer)
• Simple squamous epithelium

Figure 20-4a The Heart Wall
Mesothelium
Endocardium
Areolar tissue
Endothelium
Mesothelium
Dense fibrous layer
Pericardial cavity
Areolar tissue
Areolar tissue
Connective tissues
Cardiac muscle cells
Myocardium
(cardiac muscle tissue)
Epicardium
(visceral pericardium)

Figure 20-4b The Heart Wall
Atrial
musculature
Cardiac muscle tissue
forms concentric layers
that wrap around the
atria or spiral within the
walls of the ventricles.
Ventricular
musculature

• Cardiac Muscle Tissue
• Intercalated discs
• Interconnect cardiac muscle cells
• Secured by desmosomes
• Linked by gap junctions
• Convey force of contraction
• Propagate action potentials

Figure 20-5a Cardiac Muscle Cells
Cardiac muscle cells
Nucleus
Cardiac muscle
cell (sectioned)
Bundles of
myofibrils
Cardiac muscle cell
Mitochondria
Intercalated
disc (sectioned)
Intercalated discs

Figure 20-5b Cardiac Muscle Cells
Intercalated disc
Gap junction
Opposing plasma
membranes
Desmosomes
Structure of an intercalated disc

Figure 20-5c Cardiac Muscle Cells
Intercalated discs
Cardiac muscle tissue
Cardiac muscle tissue LM × 575

• Characteristics of Cardiac Muscle Cells
1. Small size
2. Single, central nucleus
3. Branching interconnections between cells
4. Intercalated discs

Table 20-1 Structural and Functional Differences between Cardiac Muscle Cells and Skeletal Muscle Fibers

• Internal Anatomy and Organization
• Interatrial septum separates atria
• Interventricular septum separates ventricles

• Internal Anatomy and Organization
• Atrioventricular (AV) valves
• Connect right atrium to right ventricle and left
atrium to left ventricle
• Are folds of fibrous tissue that extend into
openings between atria and ventricles
• Permit blood flow in one direction
• From atria to ventricles

• The Right Atrium
• Superior vena cava
• Receives blood from head, neck, upper limbs, and chest
• Inferior vena cava
• Receives blood from trunk, viscera, and lower limbs
• Coronary sinus
• Cardiac veins return blood to coronary sinus
• Coronary sinus opens into right atrium

• Foramen ovale
• Before birth, is an opening through interatrial septum
• Connects the two atria
• Seals off at birth, forming fossa ovalis

• Pectinate muscles
• Contain prominent muscular ridges
• On anterior atrial wall and inner surfaces of right
auricle

Figure 20-6a The Sectional Anatomy of the Heart
Descending aorta
Left common carotid artery
Left subclavian artery
Ligamentum arteriosum
Pulmonary trunk
Pulmonary valve
Left pulmonary
arteries
Left pulmonary
veins
Interatrial septum
Aortic valve
Cusp of left AV
(mitral) valve
LEFT VENTRICLE
Interventricular
septum
Trabeculae
carneae
Moderator band
Aortic arch
LEFT
ATRIUM
Brachiocephalic
trunk
Superior
vena cava
Right
pulmonary
arteries
Ascending aorta
Fossa ovalis
Opening of
coronary sinus
RIGHT ATRIUM
Pectinate muscles
Conus arteriosus
Cusp of right AV
(tricuspid) valve
Chordae tendineae
Papillary muscles
RIGHT VENTRICLE
Inferior vena cava

Figure 20-6c The Sectional Anatomy of the Heart
A frontal section, anterior view.
Inferior vena cava
RIGHT VENTRICLE
Papillary muscles
Cusps of right AV
(tricuspid) valve
Pectinate muscles
RIGHT ATRIUM
Fossa ovalis
Ascending aorta
Cusp of left AV
(bicuspid) valve
Interventricular
septum
LEFT VENTRICLE
Chordae tendineae
Left coronary artery
branches (red)
and great cardiac
vein (blue)
Cusp of aortic valve
Coronary sinus
Trabeculae carneae

• The Right Ventricle
• Free edges attach to chordae tendineae from
papillary muscles of ventricle
• Prevent valve from opening backward
• Right atrioventricular (AV) valve
• Also called tricuspid valve
• Opening from right atrium to right ventricle
• Has three cusps
• Prevents backflow

• The Right Ventricle
• Trabeculae carneae
• Muscular ridges on internal surface of right (and left)
ventricle
• Includes moderator band
• Ridge contains part of conducting system
• Coordinates contractions of cardiac muscle cells

Figure 20-6b The Sectional Anatomy of the Heart
The papillary muscles and chordae
tendinae supporting the right AV
(tricuspid) valve. The photograph
was taken from inside the right
ventricle, looking toward a light
shining from the right atrium.
Chordae tendineae
Papillary muscles

• The Pulmonary Circuit
• Conus arteriosus (superior end of right ventricle)
leads to pulmonary trunk
• Pulmonary trunk divides into left and right
pulmonary arteries
• Blood flows from right ventricle to pulmonary trunk
through pulmonary valve
• Pulmonary valve has three semilunar cusps

• The Left Atrium
• Blood gathers into left and right pulmonary veins
• Pulmonary veins deliver to left atrium
• Blood from left atrium passes to left ventricle through
left atrioventricular (AV) valve
• A two-cusped bicuspid valve or mitral valve

• The Left Ventricle
• Holds same volume as right ventricle
• Is larger; muscle is thicker and more powerful
• Similar internally to right ventricle but does not have
moderator band

• The Left Ventricle
• Systemic circulation
• Blood leaves left ventricle through aortic valve
into ascending aorta
• Ascending aorta turns (aortic arch) and becomes
descending aorta

• Structural Differences between the Left and
Right Ventricles
• Right ventricle wall is thinner, develops less pressure
than left ventricle
• Right ventricle is pouch-shaped, left ventricle is round
ANIMATION The Heart: Heart Anatomy

Figure 20-7a Structural Differences between the Left and Right Ventricles
Left
ventricle
Right
ventricle
Posterior
Fat in anterior
A diagrammatic sectional view through the heart,
showing the relative thicknesses of the two ventricles.
Notice the pouchlike shape of the right ventricle and
the greater thickness of the left ventricle.

Figure 20-7b Structural Differences between the Left and Right Ventricles
Dilated Contracted
Diagrammatic views of the ventricles just
before a contraction (dilated) and just after a
contraction (contracted).
Left
ventricle
Right
ventricle

• The Heart Valves
• Two pairs of one-way valves prevent backflow
during contraction
• Atrioventricular (AV) valves
• Between atria and ventricles
• Blood pressure closes valve cusps during ventricular
contraction
• Papillary muscles tense chordae tendineae to prevent
valves from swinging into atria

• The Heart Valves
• Semilunar valves
• Pulmonary and aortic tricuspid valves
• Prevent backflow from pulmonary trunk and aorta
into ventricles
• Have no muscular support
• Three cusps support like tripod

• Aortic Sinuses
• At base of ascending aorta
• Sacs that prevent valve cusps from sticking to
aorta
• Origin of right and left coronary arteries
ANIMATION The Heart: Valves

Figure 20-8a Valves of the Heart
Relaxedventricles
Right AV
(tricuspid)
valve (open)
Transverse Sections, Superior View,
Atria and Vessels Removed
POSTERIOR
RIGHT
VENTRICLE
Cardiac
skeleton
Left AV (bicuspid)
valve (open)
LEFT
VENTRICLE
Aortic valve
(closed)
Pulmonary
valve (closed)ANTERIOR
Aortic valve closed
When the ventricles are relaxed, the AV valves
are open and the semilunar valves are closed.
The chordae tendineae are loose, and the
papillary muscles are relaxed.

Figure 20-8a Valves of the Heart
Aortic valve
(closed)
LEFT
ATRIUM
Left AV (bicuspid)
valve (open)
Chordae
tendineae (loose)
Papillary muscles
(relaxed)
LEFT VENTRICLE
(relaxed and filling
with blood)
Pulmonary
veins
Frontal Sections through Left Atrium and Ventricle
Relaxedventricles

Figure 20-8b Valves of the Heart
Contractingventricles
Aortic valve open
RIGHT
VENTRICLE
Right AV
(tricuspid) valve
(closed)
Cardiac
skeleton
Left AV
(bicuspid) valve
(closed)
LEFT
VENTRICLE
Aortic valve
(open)
Pulmonary
valve (open)
When the ventricles are contracting, the
AV valves are closed and the semilunar
valves are open. In the frontal section
notice the attachment of the left AV valve
to the chordae tendineae and papillary
muscles.

Figure 20-8b Valves of the Heart
Contractingventricles
Aorta
Aortic sinus
LEFT
ATRIUM
Aortic valve
(open)
Left AV (bicuspid)
valve (closed)
Chordae tendineae
(tense)
Papillary muscles
(contracted)
Left ventricle
(contracted)

• Connective Tissues and the Cardiac Skeleton
• Connective Tissue Fibers
1. Physically support cardiac muscle fibers
2. Distribute forces of contraction
3. Add strength and prevent overexpansion of heart
4. Provide elasticity that helps return heart to original
size and shape after contraction

• The Cardiac Skeleton
• Four bands around heart valves and bases of
pulmonary trunk and aorta
• Stabilize valves
• Electrically insulate ventricular cells from atrial cells

• The Blood Supply to the Heart
• = Coronary circulation
• Supplies blood to muscle tissue of heart
• Coronary arteries and cardiac veins

• The Coronary Arteries
• Left and right
• Originate at aortic sinuses
• High blood pressure, elastic rebound forces blood
through coronary arteries between contractions

• Right Coronary Artery
• Supplies blood to:
• Right atrium
• Portions of both ventricles
• Cells of sinoatrial (SA) and atrioventricular nodes
• Marginal arteries (surface of right ventricle)
• Posterior interventricular artery

• Left Coronary Artery
• Supplies blood to:
• Left ventricle
• Left atrium
• Interventricular septum

• Two Main Branches of Left Coronary Artery
1. Circumflex artery
2. Anterior interventricular artery
• Arterial Anastomoses
• Interconnect anterior and posterior interventricular
arteries
• Stabilize blood supply to cardiac muscle

• The Cardiac Veins
• Great cardiac vein
• Drains blood from area of anterior interventricular artery into
coronary sinus
• Anterior cardiac veins
• Empty into right atrium
• Posterior cardiac vein, middle cardiac vein, and
small cardiac vein
• Empty into great cardiac vein or coronary sinus

Figure 20-9a Coronary Circulation
Aortic
arch
Ascending
aorta
Right coronary
artery
Atrial arteries
Anterior
cardiac veins
Small
cardiac vein
Marginal
artery
Left coronary
artery
Pulmonary
trunk
Circumflex
artery
Anterior
interventricular
artery
Great
cardiac
vein
Coronary vessels supplying
and draining the anterior
surface of the heart.

Figure 20-9b Coronary Circulation
Coronary sinus
Circumflex artery
Great cardiac vein
Marginal artery
Posterior
interventricular
artery
Posterior
cardiac
vein
Left
ventricle
Middle cardiac vein Marginal artery
Right coronary
artery
Small cardiac
vein
Coronary vessels supplying and draining
the posterior surface of the heart.

Figure 20-9c Coronary Circulation
Posterior interventricular artery
Posterior
cardiac vein
Marginal artery
Great cardiac vein
Circumflex artery
Auricle of
left atrium
Left pulmonary
veins
Left pulmonary
artery
Right pulmonary
artery
Superior
vena cava
Right pulmonary
veins
Left atrium
Right atrium
Inferior vena cava
Coronary sinus
Middle cardiac vein
Right ventricle
A posterior view of the heart; the vessels have been
injected with colored latex (liquid rubber).

Figure 20-10 Heart Disease and Heart Attacks
Narrowing of Artery
Lipid deposit
of plaque
Cross-section
Tunica
externa
Tunica
media
Cross-section
Normal Artery

• Heart Disease - Coronary Artery Disease
• Coronary artery disease (CAD)
• Areas of partial or complete blockage of coronary
circulation
• Cardiac muscle cells need a constant supply of
oxygen and nutrients
• Reduction in blood flow to heart muscle produces a
corresponding reduction in cardiac performance
• Reduced circulatory supply, coronary ischemia,
results from partial or complete blockage of coronary
arteries

• Usual cause is formation of a fatty deposit, or
atherosclerotic plaque, in the wall of a coronary
vessel
• The plaque, or an associated thrombus (clot), then
narrows the passageway and reduces blood flow
• Spasms in smooth muscles of vessel wall can further
decrease or stop blood flow
• One of the first symptoms of CAD is commonly
angina pectoris

• Angina Pectoris
• In its most common form, a temporary ischemia
develops when the workload of the heart increases
• Although the individual may feel comfortable at rest,
exertion or emotional stress can produce a sensation of
pressure, chest constriction, and pain that may radiate
from the sternal area to the arms, back, and neck

• Myocardial infarction (MI), or heart attack
• Part of the coronary circulation becomes blocked, and
cardiac muscle cells die from lack of oxygen
• The death of affected tissue creates a nonfunctional
area known as an infarct
• Heart attacks most commonly result from severe
coronary artery disease (CAD)

• Consequences depend on the site and nature of the
circulatory blockage
• If it occurs near the start of one of the coronary
arteries:
• The damage will be widespread and the heart
may stop beating
• If the blockage involves one of the smaller arterial
branches:
• The individual may survive the immediate crisis
but may have many complications such as
reduced contractility and cardiac arrhythmias

• A crisis often develops as a result of thrombus
formation at a plaque (the most common cause of an
MI), a condition called coronary thrombosis
• A vessel already narrowed by plaque formation may
also become blocked by a sudden spasm in the smooth
muscles of the vascular wall
• Individuals having an MI experience intense pain,
similar to that felt in angina, but persisting even at rest

• Pain does not always accompany a heart attack, therefore, the
condition may go undiagnosed and may not be treated before a
fatal MI occurs
• A myocardial infarction can usually be diagnosed with an ECG
and blood studies
• Damaged myocardial cells release enzymes into the circulation,
and these elevated enzymes can be measured in diagnostic
blood tests
• The enzymes include:
• Cardiac troponin T,
• Cardiac troponin I,
• A special form of creatinine phosphokinase, CK-MB

• Treatment of CAD and Myocardial Infarction
• About 25% of MI patients die before obtaining medical
assistance
• 65% of MI deaths among those under age 50 occur
within an hour after the initial infarction

• Risk Factor Modification
• Stop smoking
• High blood pressure treatment
• Dietary modification to lower cholesterol and
promote weight loss
• Stress reduction
• Increased physical activity (where appropriate)

• Drug Treatment
• Drugs that reduce coagulation and therefore the risk of
thrombosis, such as aspirin and coumadin
• Drugs that block sympathetic stimulation (propranolol or
metoprolol)
• Drugs that cause vasodilation, such as nitroglycerin
• Drugs that block calcium movement into the cardiac and
vascular smooth muscle cells (calcium channel blockers)
• In a myocardial infarction, drugs to relieve pain,
fibrinolytic agents to help dissolve clots, and oxygen

• Noninvasive Surgery
• Atherectomy
• Blockage by a single, soft plaque may be
reduced with the aid of a long, slender catheter
inserted into a coronary artery to the plaque

• Noninvasive Surgery
• Balloon angioplasty
• The tip of the catheter contains an inflatable
balloon
• Once in position, the balloon is inflated,
pressing the plaque against the vessel walls
• Because plaques commonly redevelop after
angioplasty, a fine tubular wire mesh called a
stent may be inserted into the vessel, holding it
open

• Coronary Artery Bypass Surgery (CABG)
• In a coronary artery bypass graft, a small section is
removed from either a small artery or a peripheral
vein and is used to create a detour around the
obstructed portion of a coronary artery
• As many as four coronary arteries can be rerouted
this way during a single operation
• The procedures are named according to the
number of vessels repaired, so we speak of single,
double, triple, or quadruple coronary bypasses

Normal Heart
Advanced Coronary Artery Disease
A color-enhanced DSA scan showing advanced
coronary artery disease. Blood flow to the ven-
tricular myocardium is severely restricted.
A color-enhanced digital subtraction
angiography (DSA) scan of a normal
heart.

Occluded
Coronary
Artery
Damaged
Heart
Muscle

20-2 The Conducting System
• Heartbeat
• A single contraction of the heart
• The entire heart contracts in series
• First the atria
• Then the ventricles

• Cardiac Physiology
• Two Types of Cardiac Muscle Cells
1. Conducting system
• Controls and coordinates heartbeat
2. Contractile cells
• Produce contractions that propel blood

• The Cardiac Cycle
• Begins with action potential at SA node
• Transmitted through conducting system
• Produces action potentials in cardiac muscle cells
(contractile cells)
• Electrocardiogram (ECG or EKG)
• Electrical events in the cardiac cycle can be recorded
on an electrocardiogram

• The Conducting System
• A system of specialized cardiac muscle cells
• Initiates and distributes electrical impulses that
stimulate contraction
• Automaticity
• Cardiac muscle tissue contracts automatically

• Structures of the Conducting System
• Sinoatrial (SA) node - wall of right atrium
• Atrioventricular (AV) node - junction between atria
and ventricles
• Conducting cells - throughout myocardium

• Conducting Cells
• Interconnect SA and AV nodes
• Distribute stimulus through myocardium
• In the atrium
• Internodal pathways
• In the ventricles
• AV bundle and the bundle branches

• Prepotential
• Also called pacemaker potential
• Resting potential of conducting cells
• Gradually depolarizes toward threshold
• SA node depolarizes first, establishing heart rate
ANIMATION The Heart: Conduction System

Figure 20-11a The Conducting System of the Heart
AV bundle
Components of the conducting
system
Purkinje
fibers
Bundle
branches
Atrioventricular
(AV) node
Internodal
pathways
Sinoatrial
(SA) node

Figure 20-11b The Conducting System of the Heart
Changes in the membrane potential of a pacemaker
cell in the SA node that is establishing a heart rate of
72 beats per minute. Note the presence of a
prepotential, a gradual spontaneous depolarization.
Time (sec)
Prepotential
(spontaneous depolarization)
Threshold

• Heart Rate
• SA node generates 80–100 action potentials per
minute
• Parasympathetic stimulation slows heart rate
• AV node generates 40–60 action potentials per
minute

• The Sinoatrial (SA) Node
• In posterior wall of right atrium
• Contains pacemaker cells
• Connected to AV node by internodal pathways
• Begins atrial activation (Step 1)

Figure 20-12 Impulse Conduction through the Heart (Step 1)
Time = 0
SA
node
SA node activity
and atrial
activation begin.

• The Atrioventricular (AV) Node
• In floor of right atrium
• Receives impulse from SA node (Step 2)
• Delays impulse (Step 3)
• Atrial contraction begins

Elapsed time = 50 msec
AV
node
Stimulus spreads across
the atrial surfaces and
reaches the AV node.

Bundle
branches
AV
bundle
There is a 100-msec delay
at the AV node. Atrial
contraction begins.

• The AV Bundle
• In the septum
• Carries impulse to left and right bundle branches
• Which conduct to Purkinje fibers (Step 4)
• And to the moderator band
• Which conducts to papillary muscles

Moderator
band
The impulse travels along
the interventricular septum
within the AV bundle and
the bundle branches to the
Purkinje fibers and, via the
moderator band, to the
papillary muscles of the
right ventricle.

• Purkinje Fibers
• Distribute impulse through ventricles (Step 5)
• Atrial contraction is completed
• Ventricular contraction begins

Purkinje
fibers
The impulse is distributed
by Purkinje fibers and
relayed throughout the
ventricular myocardium.
Atrial contraction is
completed, and ventricular
contraction begins.

• Abnormal Pacemaker Function
• Bradycardia - abnormally slow heart rate
• Tachycardia - abnormally fast heart rate
• Ectopic pacemaker
• Abnormal cells
• Generate high rate of action potentials
• Bypass conducting system
• Disrupt ventricular contractions

• The Electrocardiogram (ECG or EKG)
• A recording of electrical events in the heart
• Obtained by electrodes at specific body locations
• Abnormal patterns diagnose damage

• Features of an ECG
• P wave
• Atria depolarize
• QRS complex
• Ventricles depolarize
• T wave
• Ventricles repolarize

• Time Intervals between ECG Waves
• P–R interval
• From start of atrial depolarization
• To start of QRS complex
• Q–T interval
• From ventricular depolarization
• To ventricular repolarization

Figure 20-13a An Electrocardiogram
Electrode placement for
recording a standard ECG.

Figure 20-13b An Electrocardiogram
800 msec
SQ
QRS interval
(ventricles depolarize)
Millivolts
R
P–R segment
T wave
(ventricles repolarize)
R
P wave
(atria
depolarize)
S–T
segment
S–T
interval
Q–T
interval
P–R
interval

Figure 20-14 Cardiac Arrhythmias
Premature Atrial Contractions (PACs)
Paroxysmal Atrial Tachycardia (PAT)
Atrial Fibrillation (AF)
PPP
PPPPPP

Figure 20-14 Cardiac Arrhythmias
Premature Ventricular Contractions (PVCs)
Ventricular Tachycardia (VT)
Ventricular Fibrillation (VF)
PPP
P
TTT

• Contractile Cells
• Purkinje fibers distribute the stimulus to the contractile
cells, which make up most of the muscle cells in the
heart
• Resting Potential
• Of a ventricular cell about –90 mV
• Of an atrial cell about –80 mV

Figure 20-15a The Action Potential in Skeletal and Cardiac Muscle
Rapid Depolarization The Plateau Repolarization
Cause: Na+
entry
Duration: 3–5 msec
Ends with: Closure of
voltage-gated fast
sodium channels
Cause: Ca2+
entry
Duration: ~175 msec
Ends with: Closure
of slow calcium
channels
Cause: K+
loss
Duration: 75 msec
Ends with: Closure
of slow potassium
channels
Relative
refractory
period
Stimulus
Events in an action potential in a ventricular muscle
cell.
KEY
Absolute refractory
period
Relative refractory
period
Absolute refractory
period
Time (msec)
mV

Figure 20-15b The Action Potential in Skeletal and Cardiac Muscle
mV
SKELETAL
MUSCLE
CARDIAC
MUSCLE
Action potentialmV
Contraction
Tension
Time (msec)
Time (msec)
ContractionTension
Action
potential
KEY
Absolute refractory
period
Relative refractory
period
Action potentials and twitch
contractions in a skeletal muscle
(above) and cardiac muscle (below).

• Refractory Period
• Absolute refractory period
• Long
• Cardiac muscle cells cannot respond
• Relative refractory period
• Short
• Response depends on degree of stimulus

• Timing of Refractory Periods
• Length of cardiac action potential in ventricular cell
• 250–300 msec
• 30 times longer than skeletal muscle fiber
• Long refractory period prevents summation and
tetany

• The Role of Calcium Ions in Cardiac
Contractions
• Contraction of a cardiac muscle cell
• Is produced by an increase in calcium ion
concentration around myofibrils

Contractions
1. 20% of calcium ions required for a contraction
• Calcium ions enter plasma membrane during plateau
phase
2. Arrival of extracellular Ca2+
• Triggers release of calcium ion reserves from
sarcoplasmic reticulum (SR)

Contractions
• As slow calcium channels close
• Intracellular Ca2+
is absorbed by the SR
• Or pumped out of cell
• Cardiac muscle tissue
• Very sensitive to extracellular Ca2+
concentrations

• The Energy for Cardiac Contractions
• Aerobic energy of heart
• From mitochondrial breakdown of fatty acids and
glucose
• Oxygen from circulating hemoglobin
• Cardiac muscles store oxygen in myoglobin

20-3 The Cardiac Cycle
• The Cardiac Cycle
• Is the period between the start of one heartbeat
and the beginning of the next
• Includes both contraction and relaxation

• Two Phases of the Cardiac Cycle
• Within any one chamber
1. Systole (contraction)
2. Diastole (relaxation)

Figure 20-16 Phases of the Cardiac Cycle
Cardiac
cycle
370
msec
100
msec
0
msec800
msec
Start

Figure 20-16a Phases of the Cardiac Cycle
Cardiac
cycle
100
msec
0
msec800
msec
Atrial systole begins:
Atrial contraction forces a small amount of
additional blood into relaxed ventricles.
Start

Figure 20-16b Phases of the Cardiac Cycle
Cardiac
cycle
100
msec
Atrial systole ends,
atrial diastole
begins

Figure 20-16c Phases of the Cardiac Cycle
Cardiac
cycle
Ventricular systole—
first phase: Ventricular
contraction pushes AV
valves closed but does
not create enough
pressure to open
semilunar valves.

Figure 20-16d Phases of the Cardiac Cycle
Cardiac
cycle
370
msec
Ventricular systole—
second phase: As
ventricular pressure rises
and exceeds pressure
in the arteries, the
semilunar valves
open and blood
is ejected.

Figure 20-16e Phases of the Cardiac Cycle
Cardiac
cycle
370
msec
Ventricular diastole—early:
As ventricles relax, pressure in
ventricles drops; blood flows back
against cusps of semilunar valves
and forces them closed. Blood
flows into the relaxed atria.

Figure 20-16f Phases of the Cardiac Cycle
Cardiac
cycle
Ventricular
diastole—late:
All chambers are
relaxed.
Ventricles fill
passively.
800
msec

• Blood Pressure
• In any chamber
• Rises during systole
• Falls during diastole
• Blood flows from high to low pressure
• Controlled by timing of contractions
• Directed by one-way valves

• Cardiac Cycle and Heart Rate
• At 75 beats per minute (bpm)
• Cardiac cycle lasts about 800 msec
• When heart rate increases
• All phases of cardiac cycle shorten, particularly diastole

• Phases of the Cardiac Cycle
• Atrial systole
• Atrial diastole
• Ventricular systole
• Ventricular diastole

• Atrial Systole
1. Atrial systole
• Atrial contraction begins
• Right and left AV valves are open
2. Atria eject blood into ventricles
• Filling ventricles
3. Atrial systole ends
• AV valves close
• Ventricles contain maximum blood volume
• Known as end-diastolic volume (EDV)

• Ventricular Systole
4. Ventricles contract and build pressure
• AV valves close cause isovolumetric contraction
5. Ventricular ejection
• Ventricular pressure exceeds vessel pressure opening the
semilunar valves and allowing blood to leave the ventricle
• Amount of blood ejected is called the stroke volume (SV)

• Ventricular Systole
6. Ventricular pressure falls
• Semilunar valves close
• Ventricles contain end-systolic volume (ESV), about 40%
of end-diastolic volume

Figure 20-17 Pressure and Volume Relationships in the Cardiac Cycle
ATRIAL
SYSTOLE
ATRIAL
DIASTOLE
VENTRICULAR
DIASTOLE
VENTRICULAR
SYSTOLE
Stroke
volume
End-diastolic
volume
Left
ventricular
volume(mL)
Pressure
(mmHg)
Aortic valve
opens
Aorta
Left
ventricle
Left atrium Left AV
valve closes AV valves open; passive ventricular
filling occurs.
Isovolumetric relaxation occurs.
Semilunar valves close.
Ventricular ejection occurs.
Isovolumetric ventricular contraction.
Atrial systole ends; AV valves close.
Atria eject blood into ventricles.
Atrial contraction begins.
ATRIAL DIASTOLE
Time (msec)

• Ventricular Diastole
7. Ventricular diastole
• Ventricular pressure is higher than atrial pressure
• All heart valves are closed
• Ventricles relax (isovolumetric relaxation)
8. Atrial pressure is higher than ventricular pressure
• AV valves open
• Passive atrial filling
• Passive ventricular filling

Figure 20-17 Pressure and Volume Relationships in the Cardiac Cycle
ATRIAL
SYSTOLE
ATRIAL DIASTOLE
VENTRICULAR
SYSTOLE
VENTRICULAR DIASTOLE
AV valves open; passive ventricular
filling occurs.
Isovolumetric relaxation occurs.
Semilunar valves close.
Ventricular ejection occurs.
Isovolumetric ventricular contraction.
Atrial systole ends; AV valves close.
Atria eject blood into ventricles.
Atrial contraction begins.
Time (msec)
End-systolic
volume
Aortic valve
closes
Dicrotic
notch
Left AV
valve opens
Left
ventricular
volume(mL)
Pressure
(mmHg)

• Heart Sounds
• S1
• Loud sounds
• Produced by AV valves
• S2
• Loud sounds
• Produced by semilunar valves
ANIMATION The Heart: Cardiac Cycle

• S3, S4
• Soft sounds
• Blood flow into ventricles and atrial contraction
• Heart Murmur
• Sounds produced by regurgitation through valves

Figure 20-18a Heart Sounds
Aortic
valve
Pulmonary
valve
Valve location
Sounds heard
Left
AV
valve
Right
AV
valve
Placements of a stethoscope for
listening to the different sounds
produced by individual valves
Valve location
Sounds heard
Valve location
Sounds heard
Valve location
Sounds heard

Figure 20-18b Heart Sounds
Semilunar
valves close
AV valves
open
AV valves
close
“Dubb”“Lubb”
The relationship between heart sounds and key events in the
cardiac cycle
Heart sounds
Pressure
(mmHg)
Aorta
Semilunar
valves open
Left
ventricle
Left
atrium
S1
S4S4
S2
S3

20-4 Cardiodynamics
• Cardiodynamics
• The movement and force generated by cardiac
contractions
• End-diastolic volume (EDV)
• End-systolic volume (ESV)
• Stroke volume (SV)
• SV = EDV – ESV
• Ejection fraction
• The percentage of EDV represented by SV

Figure 20-19 A Simple Model of Stroke Volume
Filling
Ventricular
diastole
End-diastolic
volume (EDV)
Pumping
Ventricular
systole
Stroke
volume
End-systolic
volume
(ESV)
Start

Filling
Ventricular
diastole
When the pump handle is
raised, pressure within the
cylinder decreases, and
water enters through a
one-way valve. This
corresponds to passive
filling during ventricular
diastole.
Start

At the start of the pumping
cycle, the amount of water in
the cylinder corresponds to the
amount of blood in a ventricle
at the end of ventricular
diastole. This amount is known
as the end-diastolic volume
(EDV).
End-diastolic
volume (EDV)

Pumping
As the pump handle is
pushed down, water is forced
out of the cylinder. This cor-
responds to the period of
ventricular ejection.
Ventricular
systole

When the handle is depressed as
far as it will go, some water will
remain in the cylinder. That amount
corresponds to the end-systolic
volume (ESV) remaining in the
ventricle at the end of ventricular
systole. The amount of water
pumped out corresponds to the
stroke volume of the heart; the
stroke volume is the difference
between the EDV and the ESV.
Stroke
volume
End-systolic
volume
(ESV)

20-4 Cardiodynamics
• Cardiac Output (CO)
• The volume pumped by left ventricle in 1 minute
• CO = HR × SV
• CO = cardiac output (mL/min)
• HR = heart rate (beats/min)
• SV = stroke volume (mL/beat)

20-4 Cardiodynamics
• Factors Affecting Cardiac Output
• Cardiac output
• Adjusted by changes in heart rate or stroke volume
• Heart rate
• Adjusted by autonomic nervous system or hormones
• Stroke volume
• Adjusted by changing EDV or ESV

Figure 20-20 Factors Affecting Cardiac Output
End-systolic
volume
End-diastolic
volume
Hormones
Autonomic
innervation
STROKE VOLUME (SV) = EDV – ESVHEART RATE (HR)
CARDIAC OUTPUT (CO) = HR × SV
Factors Affecting
Heart Rate (HR)
Factors Affecting
Stroke Volume (SV)

20-4 Cardiodynamics
• Autonomic Innervation
• Cardiac plexuses innervate heart
• Vagus nerves (N X) carry parasympathetic
preganglionic fibers to small ganglia in cardiac plexus
• Cardiac centers of medulla oblongata
• Cardioacceleratory center controls sympathetic neurons
(increases heart rate)
• Cardioinhibitory center controls parasympathetic neurons
(slows heart rate)

20-4 Cardiodynamics
• Autonomic Innervation
• Cardiac reflexes
• Cardiac centers monitor:
• Blood pressure (baroreceptors)
• Arterial oxygen and carbon dioxide levels
(chemoreceptors)
• Cardiac centers adjust cardiac activity
• Autonomic tone
• Dual innervation maintains resting tone by releasing ACh and
NE
• Fine adjustments meet needs of other systems

Figure 20-21 Autonomic Innervation of the Heart
Cardioinhibitory
center
Cardioacceleratory
center
Vagal nucleus
Medulla
oblongata
Vagus (N X)
Spinal cord
Parasympathetic
Parasympathetic
preganglionic
fiber
Synapses in
cardiac plexus
Parasympathetic
postganglionic
fibers
Cardiac nerve
Sympathetic
postganglionic fiber
Sympathetic
preganglionic
fiber
Sympathetic
ganglia (cervical
ganglia and
superior thoracic
ganglia [T1–T4])
Sympathetic

20-4 Cardiodynamics
• Effects on the SA Node
• Membrane potential of pacemaker cells
• Lower than other cardiac cells
• Rate of spontaneous depolarization depends on:
• Resting membrane potential
• Rate of depolarization

Figure 20-22a Autonomic Regulation of Pacemaker Function
Prepotential
(spontaneous
depolarization)
Normal (resting)
Membrane
potential
(mV)
Threshold
Heart rate: 75 bpm
Pacemaker cells have membrane potentials closer to threshold
than those of other cardiac muscle cells (–60 mV versus
–90 mV). Their plasma membranes undergo spontaneous
depolarization to threshold, producing action potentials at a
frequency determined by (1) the resting-membrane potential
and (2) the rate of depolarization.

20-4 Cardiodynamics
• Effects on the SA Node
• Sympathetic and parasympathetic stimulation
• Greatest at SA node (heart rate)
• ACh (parasympathetic stimulation)
• Slows the heart
• NE (sympathetic stimulation)
• Speeds the heart

Figure 20-22b Autonomic Regulation of Pacemaker Function
Parasympathetic stimulation releases ACh, which
extends repolarization and decreases the rate of
spontaneous depolarization. The heart rate slows.
Slower depolarization
Hyperpolarization
Parasympathetic stimulation
Heart rate: 40 bpm
Membrane
potential
(mV)
Threshold

Figure 20-22c Autonomic Regulation of Pacemaker Function
Sympathetic stimulation releases NE, which shortens
repolarization and accelerates the rate of spontaneous
depolarization. As a result, the heart rate increases.
Time (sec)
More rapid
depolarization
Reduced repolarization
Sympathetic stimulation
Heart rate: 120 bpm
Membrane
potential
(mV)
Threshold

20-4 Cardiodynamics
• Atrial Reflex
• Also called Bainbridge reflex
• Adjusts heart rate in response to venous return
• Stretch receptors in right atrium
• Trigger increase in heart rate
• Through increased sympathetic activity

20-4 Cardiodynamics
• Hormonal Effects on Heart Rate
• Increase heart rate (by sympathetic stimulation of
SA node)
• Epinephrine (E)
• Norepinephrine (NE)
• Thyroid hormone

20-4 Cardiodynamics
• Factors Affecting the Stroke Volume
• The EDV amount of blood a ventricle contains at the
end of diastole
• Filling time
• Duration of ventricular diastole
• Venous return
• Rate of blood flow during ventricular diastole

20-4 Cardiodynamics
• Preload
• The degree of ventricular stretching during ventricular
diastole
• Directly proportional to EDV
• Affects ability of muscle cells to produce tension

20-4 Cardiodynamics
• The EDV and Stroke Volume
• At rest
• EDV is low
• Myocardium stretches less
• Stroke volume is low
• With exercise
• EDV increases
• Myocardium stretches more
• Stroke volume increases

20-4 Cardiodynamics
• The Frank–Starling Principle
• As EDV increases, stroke volume increases
• Physical Limits
• Ventricular expansion is limited by:
• Myocardial connective tissue
• The cardiac (fibrous) skeleton
• The pericardial sac

20-4 Cardiodynamics
• End-Systolic Volume (ESV)
• Is the amount of blood that remains in the ventricle
at the end of ventricular systole

20-4 Cardiodynamics
• Three Factors That Affect ESV
1. Preload
• Ventricular stretching during diastole
2. Contractility
• Force produced during contraction, at a given preload
3. Afterload
• Tension the ventricle produces to open the semilunar
valve and eject blood

20-4 Cardiodynamics
• Contractility
• Is affected by:
• Autonomic activity
• Hormones

20-4 Cardiodynamics
• Effects of Autonomic Activity on Contractility
• Sympathetic stimulation
• NE released by postganglionic fibers of cardiac nerves
• Epinephrine and NE released by adrenal medullae
• Causes ventricles to contract with more force
• Increases ejection fraction and decreases ESV

20-4 Cardiodynamics
• Effects of Autonomic Activity on Contractility
• Parasympathetic activity
• Acetylcholine released by vagus nerves
• Reduces force of cardiac contractions

20-4 Cardiodynamics
• Hormones
• Many hormones affect heart contraction
• Pharmaceutical drugs mimic hormone actions
• Stimulate or block beta receptors
• Affect calcium ions (e.g., calcium channel blockers)

20-4 Cardiodynamics
• Afterload
• Is increased by any factor that restricts arterial
blood flow
• As afterload increases, stroke volume decreases

Figure 20-23 Factors Affecting Stroke Volume
Preload
Factors Affecting Stroke Volume (SV)
Venous return (VR)
VR = EDV FT = EDV
Filling time (FT) Increased by
sympathetic
stimulation
Decreased by
parasympathetic
stimulation
Increased by E, NE,
glucagon,
thyroid hormones
Contractility (Cont)
of muscle cells
Cont = ESV Increased by
vasoconstriction
Decreased by
vasodilation
Afterload (AL)
AL = ESVEnd-systolic
volume (ESV)
End-diastolic
volume (EDV)
STROKE VOLUME (SV)
ESV = SV
VR = EDV FT = EDV
Cont = ESV
AL = ESV
ESV = SV
EDV = SV
EDV = SV

20-4 Cardiodynamics
• Summary: The Control of Cardiac Output
• Heart Rate Control Factors
• Autonomic nervous system
• Sympathetic and parasympathetic
• Circulating hormones
• Venous return and stretch receptors

20-4 Cardiodynamics
• Summary: The Control of Cardiac Output
• Stroke Volume Control Factors
• EDV
• Filling time, and rate of venous return
• ESV
• Preload, contractility, afterload

20-4 Cardiodynamics
• Cardiac Reserve
• The difference between resting and maximal
cardiac output

20-4 Cardiodynamics
• The Heart and Cardiovascular System
• Cardiovascular regulation
• Ensures adequate circulation to body tissues
• Cardiovascular centers
• Control heart and peripheral blood vessels
• Cardiovascular system responds to:
• Changing activity patterns
• Circulatory emergencies

Figure 20-24 A Summary of the Factors Affecting Cardiac Output
Hormones
Factors affecting heart fate (HR) Factors affecting stroke volume (SV)
CARDIAC OUTPUT (CO) = HR × SV
STROKE VOLUME (SV) = EDV – ESVHEART RATE (HR)
Afterload
End-systolic
volume
End-diastolic
volume
Vasodilation or
vasoconstriction
ContractilityPreload
HormonesAutonomic
innervation
Filling
time
Venous
return
Changes in
peripheral
circulation
Blood
volume
Skeletal
muscle
activity
Autonomic
innervation
Atrial
reflex

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